Chapter 4, Hemodynamic disorders, Thromboembolism, and shock

Question 1

defined hemostasis?

Answer 1

blood clotting

Question 2

thrombosis definition?

Answer 2

inappropriate clotting

Question 3

Embolism definition?

Answer 3

migration of clots which could cause ischemic cell death (infraction)

Question 4

Hyperemia definition?

Answer 4

active process resulting from arteriolar dilation and increased blood inflow (inflammation or exercising muscle)
tissue appears redder due to oxygenated blood.

Question 5

Congestion definition?

Answer 5

passive process resulting from impaired outflow of venous blood from tissues. (cardiac failure or local obstruction)
tissue appears blue due to deoxy-blood (cyanosis).

Question 6

name that is used to describe fluid accumulation in pleural cavity, pericardial cavity, or the peritoneal cavity

Answer 6

• pleural cavity (hydrothorax)
• pericardial cavity (hydropericardium)
• peritoneal cavity (hydroperitoneum or ascites)

Question 7

definition of Anasarca?

Answer 7

a severed, generalized edema marked by profound swelling of subcutaneous tissues and accumulation of fluid in body cavities.

Question 8

the does the vicious cycle of fluid retention occur during edema?

Answer 8

increased venous hydrostatic pressure in patients with congestive heart failure. The reduced cardiac output results in hypoperfusion of the kidneys, triggering the renin-angiotensin-aldosterone axis, increasing blood volume that the failing heart may not be able to compensate for. thus edema worsens.

Question 9

causes of Edema?

Answer 9

• increased hydrostatic pressure (heart failure)
• reduced plasma osmotic pressure (low albumin)
• lymphatic obstruction
• Sodium and water retention

Question 10

what are the causes of reduced plasma osmotic pressure?

Answer 10

reduced Albumin concentration which makes up upto half of the proteins in the blood.

• Nephrotic syndrome: leaky glomerular capillaries causes albumin and protein loss.
• Reduced albumin synthesis (liver disease)

Question 11

define pitting edema

Answer 11

when a finger is used to apply pressure to an edema causing a finger-shaped depression.

Question 12

define hemorrhagic diatheses

Answer 12

clinical disorders increasing the risk of hemorrhage.

extensive hemorrhage can result in jaundice from the massive RBC breakdown.

Question 13

define hemarthrosis

Answer 13

accumulation of blood in the joints.

Question 14

Petechiae definition?

Answer 14

1-2mm diameter hemorrhages into the skin, mucous membranes or serosal surfaces (low platelet count, defective platelet function, loss of vascular wall support due to low vitamin C.

Question 15

purpura definition?

Answer 15

a larger 3-5mm hemorrgaes (caused by trauma, vascular inflammation, and also the same disorders as petechiae.

Question 16

ecchymoses definition?

Answer 16

subcutaneous hematomas (a bruise)

Question 17

why does internal bleeding not lead to iron deficiency?

Answer 17

internal blood loss, the RBC are phagocytosed and the iron is efficiently recycled.

Question 18

Glanzmann thrombasthenia

Answer 18

bleeding disorder caused by GP IIBb/IIIa in platelets.

Question 19

what does Coumadin do?

Answer 19

antagonizes the enzymatic reaction that produce y-carboxylated glutamic acid using vitamin K as cofactor, it is a widely used anti-coagulant.

Question 20

prothrombin time tests what?

Answer 20

assesses the function of the proteins in the EXTRINSIC pathway.

Question 21

Partial thromboplastin time (PTT) test what?

Answer 21

Intrinsic pathway proteins function.

Question 22

function of Thrombin?

Answer 22

• conversion of fibrinogen into crosslinked fibrin
• platelet activation (via PAR protease activated receptor)
• proinflammatory effects
• anti-coagulant effects

Question 23

3 methods to prevent the coagulation plug from spreading from the site of injury?

Answer 23

1: the blood washes out the pro-coagulant factors
2: the negative charges on platelet surface is limited to site injury
3: the anticoagulant factors expressed adjacent to site of injury. (plasminogen made into plasmin via XII and tPA) a2-plasmin inhibitor, inhibits free plasmin.

Question 24

3 methods to prevent the coagulation plug from spreading from the site of injury?

Answer 24

1: the blood washes out the pro-coagulant factors
2: the negative charges on platelet surface is limited to site injury
3:

Question 25

process of the anti-coagulant effect of endothelium?

Answer 25

Thrombin binding to thrombomodulin and protein C which then cleaves factors Va and VIIIa.

Question 26

what is the Virchow’s triad?

Answer 26

in thrombosis the primary abnormalities that lead to intravascular thrombosis:

• Endothelial injury
• Abnormal blood flow
• Hypercoagulability

Question 27

how does inflammation cause coagulation?

Answer 27

endothelial cells actiavted by cytokines downregulate the expression of thrombomodulin.
inflammed endothelium can also down regulate protein C
-activated endothelium secrete plasminogen activator inhibitor (PAI), which limit firbinolysis, (inflammation can be disturbed)

Question 28

how does abnormal blood flow cause thrombosis?

Answer 28

• stasis and turbulence promote endothelial ell activation and enhanced pro-coagulant activity through flow-induced changes in endothelial gene expression.
• Stasis allows platelets and leukocytes to come into contact with the endothelium when the flow is sluggish.
• Stasis also slows the washout of activated clotting factors and impedes the inflow of clotting factor inhibitors.

Question 29

what would cause hypercoagulability?

Answer 29

• Leiden mutation

- prothrombin gene mutation

Question 30

what is Heparin-induced thrombocytopenia syndrome?

Answer 30

this syndrome occurs in up to 5% of patients treated with unfractionated heparin. marked by the development of autoantibodies that bind complexes of heparin and platelet membrane protein. the result is a prothrombic state.

Question 31

define anti-phospholipid antibody syndrome?

Answer 31

autoimmune, hypercoagulable state caused by antiphospholipid antibodies. It provokes blood clost in both arteries and veins and can result in pregnancy related complications.
The 2 antibody blood tests confirm the presence of either lupus anticoagulant.

Question 32

4 fates of the thrombus?

Answer 32

1: propagation (clot grows)
2: embolization (pieces of the clot dislodge)
3: Dissolution (clots dissolve)
4: Organization and recanalization (vessels may form through the clot re-establishing the original lumen.)

Question 33

what can an embolus be made of?

Answer 33

thrombus, fat droplets, bubbles of air or nitrogen, atherosclerotic debris, tumor fragments, bits of bone marrow, or amniotic fluid.

Question 34

arterial versus venous fromed thrombus?

Answer 34

venous usually ends up in the lungs and originates in the legs
arterial usually ends up in extremities and possibly the CNS

Question 35

Fat embolism definition?

Answer 35

during skeletal injury (fracture) small fat droplets are released into the circulation.
clinical symptoms appear 1-3 days after injury.
platelets can bind to the fat droplet

Question 36

thrombocytopenia

Answer 36

low platelet count

Question 37

what injury is caused by fat globules?

Answer 37

they can occlude vessels by triggering platelet aggregation.
the fatty acids damage the endothelium.

Question 38

Amniotic fluid embolism?

Answer 38

amniotic fluid enters the mother blood and triggers reactions. the coagulation pathway and the innate immune system.

Question 39

Red vs white infarcts

Answer 39

Red infrarcts are hemorrhagic infarcts and usually occur in less dense tissue like the lungs and GI tract. White infarcts (also called anemic infarcts) are non-hemorrhagic and are more likely in denser tissues like the myocardium (heart muscle) and other muscle tissues as well as the kidneys and spleen.

Question 40

Shock definition?

Answer 40

• cardiogenic chock
• hypovolemic shock
• septic shock (inflammation)

Question 41

Septic shock causes?

Answer 41

gram-positive bacteria followed by gram-negative bacteria and fungi.

Question 42

pathogenesis of septic shock?

Answer 42

• inflammatory and counterinflammtory responses
• endothelial activation and injury
• induction of a procoagulant state (low blood flow causes stasis)
• metabolic abnormaliteis (inflammatory mediators suppress insulin release and cause insulin resistance)
• organ dysfunction